The DOI matches its Crossref record; 160 of the 160 references it cites were found in a registry or an index.
The neurobiological basis of cognitive impairment in Parkinson's disease
Open accessAbstract
The recent formalization of clinical criteria for Parkinson's disease with dementia (PDD) codifies many studies on this topic, including those assessing biological correlates. These studies show that the emergence of PDD occurs on the background of severe dopamine deficits with, the main pathological drivers of cognitive decline being a synergistic effect between alpha‐synuclein and Alzheimer's disease pathology. The presence of these pathologies correlates with a marked loss of limbic and cortically projecting dopamine, noradrenaline, serotonin, and acetylcholine neurons, although the exact timing of these relationships remains to be determined. Genetic factors, such as triplications in the α‐synuclein gene, lead to a clear increased risk of PDD, whereas others, such as parkin mutations, are associated with a reduced risk of PDD. The very recent formalization of clinical criteria for PD with mild cognitive impairment (PD‐MCI) allows only speculation on its biological and genetic bases. Critical assessment of animal models shows that chronic low‐dose MPTP treatment in primates recapitulates PD‐MCI over time, enhancing the current biological concept of PD‐MCI as having enhanced dopamine deficiency in frontostriatal pathways as well as involvement of other neurotransmitter systems. Data from other animal models support multiple transmitter involvement in cognitive impairment in PD. Whereas dopamine dysfunction has been highlighted because of its obvious role in PD, the role of the other neurotransmitter systems, neurodegenerative pathologies, and genetic factors in PD‐MCI remains to be fully elucidated. © 2014 International Parkinson and Movement Disorder Society
Overview
The claims and statistics of this paper haven’t been checked yet.
Run the check — free, no account needed. It reads the open-access text and checks the sources it cites.
Integrity signals
Registry
Cites
Statistics
Verification
Claims the paper makes
The claims and statistics of this paper haven’t been checked yet.
Run the check — free, no account needed. It reads the open-access text and checks the sources it cites.
Self-check
Percentages, sums and reported differences re-computed from the paper’s own numbers.
The self-check needs the paper’s full text.
Citations
Cites
α-Synuclein Locus Triplication Causes Parkinson's Disease
Singleton, A. B., Farrer, M., Johnson, J., Singleton, A., Hague, S., Kachergus, J., Hulihan, M., Peuralinna, T., Dutra, A., Nussbaum, R., et al. (2003) · Science · doi:10.1126/science.1090278 · Cited by 4,383
Self-citationClinical diagnostic criteria for dementia associated with Parkinson’s disease
Emre, M., Aarsland, D., Brown, R., Burn, D. J., Duyckaerts, C., Mizuno, Y., Broe, G. A., Cummings, J., Dickson, D. W., Gauthier, S., et al. (2007) · Movement Disorders · doi:10.1002/mds.21507 · Cited by 3,027
The new mutation, E46K, of α‐synuclein causes parkinson and Lewy body dementia
Zarranz, J. J., Alegre, J., Gómez‐Esteban, J. C., Lezcano, E., Ros, R., Ampuero, I., Vidal, L., Hoenicka, J., Rodriguez, O., Atarés, B., et al. (2004) · Annals of Neurology · doi:10.1002/ana.10795 · Cited by 2,737
Litvan, I., Goldman, J. G., Tröster, A. I., Schmand, B. A., Weintraub, D., Petersen, R. C., Mollenhauer, B., Adler, C. H., Marder, K., Williams‐Gray, C. H., et al. (2012) · Movement Disorders · doi:10.1002/mds.24893 · Cited by 2,609
Self-citationThe Sydney multicenter study of Parkinson's disease: The inevitability of dementia at 20 years
Hely, M. A., Reid, W. G. J., Adena, M. A., Halliday, G. M., & Morris, J. G. L. (2008) · Movement Disorders · doi:10.1002/mds.21956 · Cited by 2,246
Self-citationMulticenter Analysis of Glucocerebrosidase Mutations in Parkinson's Disease
Sidransky, E., Nalls, M. A., Aasly, J. O., Aharon-Peretz, J., Annesi, G., Barbosa, E. R., Bar-Shira, A., Berg, D., Bras, J., Brice, A., et al. (2009) · New England Journal of Medicine · doi:10.1056/nejmoa0901281 · Cited by 2,135
α-synuclein locus duplication as a cause of familial Parkinson's disease
Chartier-Harlin, M.-C., Kachergus, J., Roumier, C., Mouroux, V., Douay, X., Lincoln, S., Levecque, C., Larvor, L., Andrieux, J., Hulihan, M., et al. (2004) · The Lancet · doi:10.1016/s0140-6736(04)17103-1 · Cited by 2,029
The hippocampal-VTA loop: controlling the entry of information into long-term memory
Lisman, J. E., & Grace, A. A. (2005) · Neuron · doi:10.1016/j.neuron.2005.05.002 · Cited by 1,983
Genome-wide association study reveals genetic risk underlying Parkinson's disease
Simón-Sánchez, J., Schulte, C., Bras, J. M., Sharma, M., Gibbs, J. R., Berg, D., Paisan-Ruiz, C., Lichtner, P., Scholz, S. W., Hernandez, D. G., et al. (2009) · Nature Genetics · doi:10.1038/ng.487 · Cited by 1,751
Satake, W., Nakabayashi, Y., Mizuta, I., Hirota, Y., Ito, C., Kubo, M., Kawaguchi, T., Tsunoda, T., Watanabe, M., Takeda, A., et al. (2009) · Nature Genetics · doi:10.1038/ng.485 · Cited by 1,324
Cited by
Non-motor features of Parkinson disease
Schapira, A. H. V., Chaudhuri, K. R., & Jenner, P. (2017) · Nature Reviews Neuroscience · doi:10.1038/nrn.2017.62 · Cited by 2,053
Cognitive decline in Parkinson disease
Aarsland, D., Creese, B., Politis, M., Chaudhuri, K. R., ffytche, D. H., Weintraub, D., & Ballard, C. (2017) · Nature Reviews Neurology · doi:10.1038/nrneurol.2017.27 · Cited by 1,027
Parkinson’s disease dementia: a neural networks perspective
Gratwicke, J., Jahanshahi, M., & Foltynie, T. (2015) · Brain · doi:10.1093/brain/awv104 · Cited by 435
Insulin resistance and Parkinson’s disease: A new target for disease modification?
Athauda, D., & Foltynie, T. (2016) · Progress in Neurobiology · doi:10.1016/j.pneurobio.2016.10.001 · Cited by 328
Dementia with Lewy bodies and Parkinson’s disease-dementia: current concepts and controversies
Jellinger, K. A. (2018) · Journal of Neural Transmission · doi:10.1007/s00702-017-1821-9 · Cited by 264
Metadata
- Authors
- Halliday, G. M., Leverenz, J. B., Schneider, J. S., & Adler, C. H.
- Venue
- Movement Disorders
- Publisher
- Wiley
- Published
- 2014-04-15
- Volume
- 29
- Issue
- 5
- Pages
- 634-650
- ISSN
- 0885-3185 (ISSN-L)
- 1531-8257
- OpenAlex
- W1672024307
- Cited by
- 366
- References
- 160
- FWCI
- 18.82
- Type
- journal article
- Language
- en
- Open access
- green
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
Statistics and arithmetic are recomputed, not judged.
Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.
What counts as a claim ›How we measure confidence ›How we check this ›
Are you an author, or do you see a problem with this page? Request a review
How to cite
Cite CoChat for the checks on this page, and the paper for its own findings.
- This page
- CoChat. (2026). Citation check: The neurobiological basis of cognitive impairment in Parkinson's disease. https://app.cochat.ai/papers/10.1002/mds.25857
- The paper
- Halliday, G. M., Leverenz, J. B., Schneider, J. S., & Adler, C. H. (2014). The neurobiological basis of cognitive impairment in Parkinson's disease. Movement Disorders. https://doi.org/10.1002/mds.25857
Data sources
Bibliographic data: Semantic Scholar, OpenAlex, Crossref.
Contains information from the Semantic Scholar Academic Graph Datasets, made available under the ODC Attribution License (ODC-BY 1.0).
Semantic Scholar’s data is described in: Kinney, R., et al. (2023). The Semantic Scholar Open Data Platform. arXiv:2301.10140.
